Suppression of cardiac phenotypes in Rae28^–/– embryos by overexpression of NKX2.5. (a and b) Whole-mount in situ hybridization of 9.5-dpc embryos with a NKX2.5 probe. Since we used a human NKX2.5 probe, the signal in the wild-type embryo was weaker, while that from the transgene was detected clearly. (c–f) Histological sections of the mutant hearts. The offspring were generated by intercrossing of Rae28^+/– mice carrying the NKX2.5 transgene, and the hearts derived from Rae28^–/– embryos with or without the transgene were examined histologically. (g–j) Whole-mount in situ hybridization of 9.5-dpc embryos with a Hand1 probe. The findings were reproducible in the other embryo with the same genotype (data not shown). WT, wild-type embryos; –/–, Rae28^–/– embryos; NKX, NKX2.5 transgenic embryos; –/–&NKX, Rae28^–/– embryos carrying the NKX2.5 transgene; LM, lateral mesoderm. Scale bar: 500 μm.